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A Algra

Publications and source records attributed to A Algra.

At least 181 records · Page 10Linked to original sources
PubMed1996

Risk of primary sclerosing cholangitis is associated with nonsmoking behavior.

BACKGROUND & AIMS: Seventy percent of patients with primary sclerosing cholangitis (PSC) have concomitant ulcerative colitis. Smoking and previous appendectomy may protect against ulcerative colitis. The aim of this study was to examine these factors in patients with PSC. METHODS: Fifty-nine patients with PSC, 130 patients with ulcerative colitis and normal liver biochemistry, and 197 control subjects were interviewed about smoking behavior and history of appendectomy. RESULTS: There were less current smokers in the PSC and ulcerative colitis groups than in the control group (19%, 12%, and 38%, respectively). The resulting odds ratio for current smoking was 0.37 (95% confidence interval, (0.18-0.76) in the PSC group and 0.23 (95% confidence interval, 0.13-0.41) in the ulcerative colitis group. Percentage of persons who ever smoked was also significantly less in the PSC group (41% vs. 56% in the control group). Frequency of previous appendectomy in the PSC and ulcerative colitis groups was not significantly different from that of controls (19%, 9%, and 14%, respectively). CONCLUSIONS: Smoking but not previous appendectomy is associated with decreased risk of PSC.

Adult↗
PubMed1996

Welder identity, weld date, and the risk of outlet strut fracture in Björk-Shiley convexo-concave valves: the Dutch cohort study.

OBJECTIVE: To establish whether there is an association between subsequent fracture of the outlet strut and welder identity and the weld date of Björk-Shiley convexo-concave (BScc) valves. DESIGN: Cohort study. PATIENTS: All Dutch BScc valve recipients (n = 2266). MEAN OUTCOME MEASURES: Documented outlet strut fracture during follow up. RESULTS: Weld dates were known for 97.0% of all BScc valves (n = 2534) implanted in Dutch patients (n = 2266) and welder identity was known for 52.2%. During a mean follow up of 9.4 years, 46 fractures were documented. For 60 degrees valves welded from 1981 to 1984 the fracture rate (0.22 per 100 person-years (95% CI 0.13 to 0.34)) was higher than that for valves welded before 1981 (0.04 (95% CI 0.01-0.10)). When all fracture related risk factors were taken into account, fracture rates per welder did not show any statistically significant differences. CONCLUSIONS: Welder identity does not contribute to the risk of strut fracture. Other factors in the production of BScc valves may explain the increased risk for valves welded from 1981 to 1984.

Cohort Studies↗
PubMed1996

Aspirin at any dose above 30 mg offers only modest protection after cerebral ischaemia.

There is continuing debate about the relative efficacy of low (< 100 mg per day), medium (300 to 325 mg per day), and high (> 900 mg per day) doses of aspirin in patients after a transient ischaemic attack or non-disabling stroke. The purpose of this study was to resolve the issue. Thus a minimeta-analysis was performed on data from 10 randomised trials of aspirin only v control treatment in 6171 patients after a transient ischaemic attack or nondisabling stroke. The data on the trials were listed in an appendix of the report on the second cycle of the Antiplatelet Trialists' Collaboration. There was virtually no difference in relative risk reduction for low, medium, and high doses of aspirin (13%, 9%, and 14% respectively). This equivalence corresponds with the results of the UK-TIA trial in a direct comparison of 300 and 1200 mg. The Dutch TIA trial showed no difference in efficacy of 30 and 283 mg. It is concluded that aspirin at any dose above 30 mg daily prevents 13% (95% confidence interval 4-21) of vascular events and that there is a need for more efficacious drugs.

Aspirin↗
PubMed1996

Wilson disease: findings at MR imaging and CT of the brain with clinical correlation.

PURPOSE: To describe the spectrum of brain abnormalities in Wilson disease (hepatolenticular degeneration) as depicted at magnetic resonance (MR) imaging and computed tomography (CT) and to relate these findings to neurologic and hepatologic abnormalities. MATERIALS AND METHODS: Fifty patients with Wilson disease participated in the cross-sectional study: Patients underwent cerebral MR imaging (n = 49), CT (n = 44), abdominal duplex ultrasound (US) (n = 46), and neurologic examination (n = 50) within a week. Relative risk and the Fisher exact test were used for statistical analysis. RESULTS: Supratentorial and infratentorial abnormalities in the gray and white matter were found in the pyramidal and extrapyramidal system. In Wilson disease, an abnormal striatum depicted on MR images correlated with pseudoparkinsonian signs, an abnormal dentatothalamic tract correlated with cerebellar signs, and an abnormal pontocerebellar tract correlated with pseudoparkinsonian signs. The presence of portosystemic shunt was strongly associated with abnormality of the globus pallidus. CONCLUSION: MR imaging findings were of some use in the clinical treatment of patients with Wilson disease.

Adult↗
PubMed1996

Hypertension, stroke, and coronary heart disease in relatives of patients with subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: First-degree relatives of patients with subarachnoid hemorrhage (SAH) have a three to seven times greater risk of SAH than second-degree relatives and than the general population. If hypertension, which is in part genetically determined, contributes to this increased risk, the frequency of hypertension and its sequelae would be expected to be higher in first- than in second-degree relatives of patients with SAH. METHODS: We compared the reported frequency of hypertension, stroke, and coronary heart disease between 1290 first- and 3588 second-degree relatives of a prospective series of patients with SAH. RESULTS: The relative risk adjusted for age and survival status in first-degree relatives was 2.3 (95% confidence interval [CI], 1.9 to 2.9) for hypertension, 1.8 (95% CI, 1.3 to 2.4) for stroke, and 1.9 (95% CI, 1.5 to 2.3) for coronary heart disease. CONCLUSIONS: Hypertension is a familial factor contributing to the risk of SAH. Hypertension should be sought and treated in first-degree relatives of patients with SAH to reduce the increased risk of cerebrovascular and cardiovascular diseases.

Adolescent↗
PubMed1996

Risk factors for subarachnoid hemorrhage: a systematic review.

BACKGROUND AND PURPOSE: Knowledge of modifiable risk factors for subarachnoid hemorrhage (SAH) is important in terms of prevention. We therefore conducted a systematic review of studies on risk factors for SAH, with emphasis on sufficiently precise criteria for the diagnosis of SAH. METHODS: To identify studies we performed a Medline search from 1966 to 1994 and searched the reference lists of all relevant publications. Studies were included only if they fulfilled predefined methodological criteria. Case-control studies were included if the diagnosis of SAH was proved by CT, angiography, or autopsy in at least 70% of patients. Longitudinal studies were included if the criteria for SAH were based on a review of the medical records. RESULTS: Nine longitudinal studies and 11 case-control studies were included. Significant risk factors were as follows: (1) smoking (relative risk [RR] for longitudinal studies, 1.9; 95% confidence interval [CI], 1.5 to 2.3; odds ratio [OR] for case-control studies, 3.5; 95% CI, 2.9 to 4.3); (2) hypertension (RR, 2.8; 95% CI, 2.1 to 3.6; OR, 2.9; 95% CI, 2.4 to 3.7) and (3) drinking 150 g or more of alcohol per week (RR, 4.7; 95% CI, 2.1 to 10.5; OR, 1.5; 95% CI, 1.1 to 1.9). Use of oral contraceptives, hormone replacement therapy, hypercholesterolemia, and physical activity were not significantly related to the risk of SAH. CONCLUSIONS: We conclude that smoking, hypertension, and alcohol abuse are important risk factors for SAH. Reduction of exposure to these risk factors might result in a decreased incidence of SAH.

Alcohol Drinking↗
PubMed1996

Incidence of subarachnoid hemorrhage: role of region, year, and rate of computed tomography: a meta-analysis.

BACKGROUND AND PURPOSE: The incidence of subarachnoid hemorrhage (SAH) has been estimated for many years at 10 to 15 per 100 000 person-years, but the most recent studies yield lower figures, of 6 to 8 per 100 000 person-years. To investigate the cause of this apparent decline, we studied the influence of year to study, rate of CT,and region. RESULTS: Eighteen studies fulfilled predefined inclusion criteria. In three Finnish studies, the pooled incidence was 21.4 per 100 000 person-years (95% confidence interval [CI], 19.5 to 23.4); in 15 non-Finnish studies, it was 7.8 per 100 000 person-years (95% CI, 7.2 to 8.4). With univariate analysis, in non-Finnish studies the incidence decreased .96% for each percentage point increase of patients investigated with CT (rate ratio, -0.9904; 95% CI, 0.9878 to 0.9930). With 100% CT scanning, the incidence of SAH outside Finland is estimated at 6 per 100 000 person-years. The rate ratio for year of study was 0.952 (95% CI, 0.935 to 0.969) for each later year in the period 1960 to 1994. In multivariate analysis, only the use of CT was independently related to SAH incidence. For the Finnish studies, the rate ratios for use of CT and year to study were not statistically significant. We also found in six studies that incidence for women was 1.6 (95% CI, 1.1 to 2.3) times higher than that for men (7.1 [95% CI, 5.4 to 8.7] and 4.5 [95% CI, 3.1 to 5.8], respectively). CONCLUSIONS: The actual incidence of SAH has remained stable over the last three decades; the apparent decline in incidence is entirely explained by the greater proportion of patients investigated with CT. The incidence of SAH in Finland is almost three times as high as in other parts of the world.

Analysis of Variance↗
PubMed1996

Validation of family history in subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: In 6% to 9% of patients with subarachnoid hemorrhage (SAH), familial aggregation occurs; truly familial cases carry a worse prognosis than sporadic cases and raise the question of screening. If relatives have died from SAH, the family history is often the only available clue to the diagnosis, but the sensitivity and predictive value of such a history for SAH are unknown. METHODS: We contacted a next of kin for a consecutive series of patients who had died in the hospital of subarachnoid hemorrhage (n=20), intracerebral hemorrhage (n=22), or ischemic stroke (n=23) between 3 and 5 years previously, and we compared the diagnosis based on the history from this next of kin with the medical diagnosis confirmed by a CT scan. RESULTS: The positive predictive value of the diagnosis of "probable SAH" from the history in our study sample was 0.7; when adjusted for incidence rates in the general population it was 0.6 (95% confidence interval, 0.3 to 0.8). The sensitivity of the diagnosis based on the history was 0.5 (95% confidence interval. 0.3 to 0.7); 10 of the 20 cases of SAH were not identified. CONCLUSIONS: The family history of SAH, without confirmation from medical documents, is an insufficiently accurate tool to prove or disprove the diagnosis of familial SAH.

Cerebral Hemorrhage↗
PubMed1995

Randomized study of implantable defibrillator as first-choice therapy versus conventional strategy in postinfarct sudden death survivors.

BACKGROUND: In retrospective studies of sudden cardiac death survivors, the implantable cardioverter-defibrillator (ICD) compares favorably with medical and surgical therapy. Thus, use of the conventional strategy of starting treatment with antiarrhythmic drugs (AD), at least in certain patient categories, may be questionable. The goal of this study was to analyze the effectiveness of ICD implantation as first-choice therapy versus the conventional therapeutic strategy of starting with AD. METHODS AND RESULTS: Sixty consecutive survivors of cardiac arrest caused by old myocardial infarction were randomly assigned early ICD implantation (n = 29) or conventional therapy (n = 31). Baseline characteristics were similar in the two groups. Therapy in each patient was always guided by ECG monitoring, exercise testing, and programmed electrical stimulation (PES). Primary end points (main outcome events, including death, recurrent cardiac arrest, and cardiac transplantation), number of invasive procedures and antiarrhythmic therapy changes, and duration of hospitalization were compared. Median follow-up was 24 months (mean, 27 months). In the early ICD group, 4 patients (14%) died, all of cardiac causes. In the conventional group, 20 patients failed AD and subsequently underwent map-guided ventricular tachycardia (VT) surgery (6 patients) or ICD implantation (14 patients). Of the 6 VT surgery patients, 1 died, 1 had cardiac transplantation, and 1 had an ICD implantation because of persistent inducibility despite the addition of AD. Of the 11 patients who remained on AD as sole therapy, 2 died in the hospital before they could be retested by PES, leaving 9, judged adequately protected by AD alone. Of those, 5 died, and 1 survived recurrent cardiac arrest followed by ICD implantation. In total, 16 conventionally treated patients ended up with late ICD implantation, 3 of whom died. Thus, total mortality in the conventional group was 11 patients (35%): 4 died suddenly, 5 died of heart failure, and 2 died of noncardiac causes. Comparison of the main outcome events in both strategies showed a significant difference in favor of early ICD implantation (hazard ratio, 0.27; 95% CI, 0.09 to 0.85; P = .02). In addition, the early ICD group underwent fewer invasive procedures (median, 1 versus 3; P < .0001), had less therapy changes (P < .0001), and spent fewer days in hospital (median, 34 versus 49; P = .02). CONCLUSIONS: These data suggest that ICD implantation as first choice is preferable to the conventional approach in survivors of cardiac arrest caused by old myocardial infarction. Conventionally treated patients are likely to end up with an ICD, and those who remain on AD as sole therapy have a high risk of death regardless of efficacy assessment, including PES.

Anti-Arrhythmia Agents↗
PubMed1995

Familial subarachnoid hemorrhage: distinctive features and patterns of inheritance.

To delineate the distinctive features of familial subarachnoid hemorrhage, we compared gender and age at the time of subarachnoid hemorrhage, as well as site and number of aneurysms, in patients with familial subarachnoid hemorrhage (at least 1 first-degree relative with subarachnoid hemorrhage) and patients with sporadic subarachnoid hemorrhage (no subarachnoid hemorrhage in first- or second-degree relatives), in a prospective, hospital-based series of patients. In addition we studied the pattern of inheritance in 17 families with familial subarachnoid hemorrhage. Mean age at the time of hemorrhage in patients with the familial form was 6.8 years lower than that in those with the sporadic form, and middle cerebral artery aneurysms occurred more often in patients with familial disease. Sex distribution and number of aneurysms were similar in the two groups. Inheritance was compatible with autosomal dominant transmission in some families, and with autosomal recessive or multifactorial transmission in others. In our 5 families as well as in all 18 previously reported families with two affected generations, the age at the time of subarachnoid hemorrhage was invariably lower in later generations, which is suggestive of anticipation. We conclude that familial subarachnoid hemorrhage is a separate entity with occurrence at a young age, predilection for aneurysms of the middle cerebral artery, and variable modes of inheritance, including autosomal dominant inheritance with possible anticipation.

Adult↗
PubMed1995

Long-term surveillance by duplex scanning of nonrevised infragenicular graft stenosis.

To define the prognosis of nonrevised graft stenosis, we studied 68 infragenicular bypass grafts in patients entered into our duplex surveillance program between 1986 and 1987. Patients were grouped according to the grade of stenosis as follows: grade I = < 50% stenosis, grade II = 50% to 75% stenosis, and grade III = 75% to 99% stenosis. Time until maximum stenosis was stratified into three intervals (< 3 months, between 3 and 12 months, and > 12 months). Cumulative patency rates from the time of maximum stenosis to failure were calculated using Kaplan-Meier analysis. Fifty-three grafts (78%) developed stenoses: 10 with grade I, 25 with grade II, and 18 with grade III stenosis. Eighty-nine percent of the 18 graft occlusions occurred within 2 years. Two grafts occluded after 2 years without any severe stenosis or preceding clinical signs. During follow-up 15 nonrevised stenosed grafts (four with grade I, five with grade II, and six with grade III stenosis) remained patent longer than 2 years with a mean follow-up of 72 months. Statistical analysis for graft failure determined that grade II to III stenoses led to graft occlusion significantly earlier than grade 0 to I stenoses (p = 0.017). If graft failures resulting from revision were separated from the analysis, the time interval from operation to maximum stenosis (within 1 year) remained marginally significant for predicting occlusion, whereas no correlation was found between the grade of maximum stenosis and occlusion. Thus the prognosis for graft stenosis depends on the grade of stenosis and on the time interval from operation to stenosis. Therefore duplex surveillance seems to be most important within the first 24 months only, but is of little use in predicting impending graft failure beyond 2 years in asymptomatic patients.

Adult↗
PubMed1995

Recurrent stroke after transient ischaemic attack or minor ischaemic stroke: does the distinction between small and large vessel disease remain true to type? Dutch TIA Trial Study Group.

The incidence and vascular type of recurrent ischaemic stroke was studied in patients with supratentorial transient ischaemic attacks or non-disabling ischaemic strokes, who were treated with aspirin (30 or 283 mg). Patients were divided into groups with small vessel disease (SVD) (n = 1216) or large vessel disease (LVD) (n = 1221) on the grounds of their clinical features and CT at baseline. Patients with evidence of both SVD and LVD (n = 180) were excluded from further analyses. During follow up (mean 2.6 years) annual stroke rate was 3.6% in both groups. Of the 107 patients with SVD at baseline who had recurrent strokes, 83 proved to have an identifiable infarct: 30 (28%) again had a small vessel infarct, 39 (36%) had a large vessel ischaemic stroke and in 14 (13%) the recurrent ischaemic stroke was in the posterior fossa. Of the 110 patients with LVD at baseline and recurrent stroke, 91 had an identifiable infarct: 67 (61%) again had a large vessel ischaemic stroke, 16 (15%) had a small vessel ischaemic stroke, and eight (7%) had the recurrent ischaemic stroke in the posterior fossa. Thus patients with a transient ischaemic attack or non-disabling ischaemic stroke caused by LVD were more likely to have an ischaemic stroke of the same vessel type during follow up than patients with SVD (relative risk 2.2; 95% confidence interval 1.5-3.4). Possible explanations for this difference are: (1) patients with a small vessel ischaemic stroke at baseline had both SVD and LVD or were misdiagnosed; (2) recurrent small vessel ischaemic stroke may have occurred more often than reported, because they were silent or only minimally disabling; (3) recurring large vessel ischaemic strokes occurring in patients initially diagnosed as having SVD might have been related to potential cardiac sources of emboli that had not been previously recognized; (4) the antiplatelet drug aspirin (30 or 283 mg) prescribed in this patient group may have prevented thrombosis in small vessels better than in large vessels.

Aged↗
PubMed1995

Comparison of CT in patients with cerebral ischaemia with or without non-rheumatic atrial fibrillation. European Atrial Fibrillation Trial and Dutch T I A Trial Study Groups.

In an attempt to distinguish between the CT characteristics of strokes of presumed cardioembolic origin and strokes caused by arterial disease, a comparison was made between the baseline CT of two prospective cohorts of patients with transient ischaemic attack or minor ischaemic stroke, with (n = 985) or without (n = 2987) non-rheumatic atrial fibrillation (NRAF). Of the patients with NRAF 54% had evidence of cerebral infarction v 41% of the controls (patients with sinus rhythm (SR); odds ratio (OR) 1.7; 95% confidence interval (95% CI) 1.4-1.9). Patients with NRAF more often had multiple infarcts (OR 1.4; 95% CI 1.1-1.8), and more often infarcts that were not related to current neurological symptoms (OR 1.5; 95% CI 1.2-1.8). For symptomatic infarcts, patients with NRAF more often had cortical end zone infarcts (OR 3.1; 95% CI 2.6-3.8) and cortical border zone infarcts (OR 1.9; 95% CI 1.3-2.9) than patients with SR. Conversely, symptomatic small deep infarcts (lacunae) were more often seen in patients with SR (OR 3.9; 95% CI 2.8-5.4). Multivariate analyses showed that all these findings were independent of differences in baseline characteristics between the two study groups. The CT characteristics overlapped and did not allow a reliable distinction between cardioembolic and atherosclerotic causes of stroke in patients with NRAF.

Aged↗
PubMed1995

Predictors of major vascular events in patients with a transient ischemic attack or minor ischemic stroke and with nonrheumatic atrial fibrillation. European Atrial Fibrillation Trial (EAFT) Study Group.

BACKGROUND AND PURPOSE: The risk of major vascular events after an initial episode of cerebral ischemia in patients with nonrheumatic atrial fibrillation (NRAF) varies from 2% to 15% in the first year and is approximately 5% yearly thereafter. Few studies have reported on risk factors that can be used to identify high-risk subgroups within this patient population. METHODS: We studied the predictive value of several easily obtainable clinical characteristics in a group of 375 placebo-treated patients with NRAF and a recent episode of transient or nondisabling cerebral ischemia who were entered in a multicenter clinical trial. The mean follow-up was 1.6 years. RESULTS: By means of multivariate modeling, six independent variables were identified: history of previous thromboembolism, ischemic heart disease, enlarged cardiothoracic ratio on chest roentgenogram, systolic blood pressure greater than 160 mm Hg at study entry, NRAF for more than 1 year, and presence of an ischemic lesion on CT scan. These variables could also be used to stratify patients in low-, medium-, and high-risk subgroups for the other two arms of the trial, those treated with anticoagulation and aspirin. Patients older than 75 years with three or more risk factors seemingly benefited less from both aspirin and anticoagulant treatment. CONCLUSIONS: Easily obtainable patient characteristics are helpful in estimating the potential effect of adequate secondary prevention in patients with NRAF who recently suffered a transient ischemic attack or minor ischemic stroke.

Aged↗
PubMed1995

Outcome in familial subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: The outcome of subarachnoid hemorrhage in patients with familial occurrence of subarachnoid hemorrhage (familial SAH) is an important but neglected factor in balancing the risks of screening for asymptomatic aneurysms and repairing these in unaffected members of such families. METHODS: We studied the outcome of familial SAH in a prospective, hospital-based series of patients with at least one first-degree relative with SAH and compared it with the outcome in a prospectively collected hospital series of patients selected for the absence of SAH in first- and second-degree relatives. Outcome was graded in three categories: independence, dependence, or death. Poor outcome was defined as death or dependence. RESULTS: Of 29 patients with familial SAH, 52% had a poor outcome, whereas only 37% of 125 patients with sporadic SAH had a poor outcome. The crude relative risk for poor outcome in familial SAH was 1.4 (95% confidence interval [CI], 0.9 to 2.1; P = .14); the odds ratio adjusted for age and sex was 2.5 (95% CI, 1.0 to 6.0; P = .04). This risk is probably an underestimation due to our strict patient selection criteria. CONCLUSIONS: Patients with familial SAH have a greater risk of poor outcome than patients with sporadic SAH. This adds to the factors in favor of screening unaffected first-degree relatives of patients with familial SAH.

Adult↗